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1 eams such as EMLA (Eutectic mixture of local anaesthetics).
2  the treatment of varicose veins under local anaesthetic.
3 y invasive varicose vein surgery under local anaesthetic.
4 ective even when patients were under general anaesthetic.
5 dergo multiparametric MRI and have a general anaesthetic.
6  expulsion without the need for a surgeon or anaesthetic.
7  vagus nerve by topical application of local anaesthetic.
8  the prolongation of mIPSCs produced by this anaesthetic.
9  anorectal physiology, and examination under anaesthetic.
10  underwent sequential TBLC and SLB under one anaesthetic.
11 nal anaesthetic or sevoflurane-based general anaesthetic.
12 viours and fish should not seek to avoid the anaesthetic.
13 ients do not respond to treatment with local anaesthetics.
14 clear clinical advantages over other current anaesthetics.
15 he pH-sensitive current was blocked by local anaesthetics.
16 ribute to some important clinical effects of anaesthetics.
17 t ML-based model solves electrode fouling of anaesthetics.
18 s, gastrointestinal hormone disruptions, and anaesthetics.
19 sitivity of the RYR to caffeine and volatile anaesthetics.
20 on dependent, but comparable between the two anaesthetics.
21 A receptors by structurally distinct general anaesthetics.
22 echanism of action of general (inhalational) anaesthetics.
23 ctors of successful weaning from intravenous anaesthetics.
24 ability and the activation of the channel by anaesthetics.
25 soelectricity that can be induced by general anaesthetics.
26  individual variability in susceptibility to anaesthetics.
27 66-0.93; p=0.005), and spinal versus general anaesthetic (0.85, 0.74-0.97; p=0.019).
28 that are essential for responses to volatile anaesthetics(10), neurotransmitters(13) and G-protein-co
29                                          The anaesthetic 2,6-diisopropylphenol (propofol, 3 microM) a
30 xposure to intraluminal application of local anaesthetic (2 % Xylocaine).
31 enges to antibiotics [40/44 (91%]) and local anaesthetics [41/44 (93%)].
32  rate of any maternal death was 9.8 per 1000 anaesthetics (5.2-15.7, I(2)=92%) when managed by non-ph
33 eep/wake cycles(8) and responses to volatile anaesthetics(8-11).
34                                    All three anaesthetics accelerated the rate of re-entrant excitati
35  and neurophysiological analyses of volatile anaesthetic action in Drosophila, and suggest candidate
36                     The mechanism of general anaesthetic action is only partially understood.
37 echanistic basis for the genetic analysis of anaesthetic action, by analysing the neurophysiological
38                      These data suggest that anaesthetic actions resulting from effects on either TAS
39                                   Beyond its anaesthetic actions, however, the effects of ketamine on
40                           The discovery that anaesthetics affect a recently identified family of pota
41        Preclinical data suggest that general anaesthetics affect brain development.
42    A modified technique for estimating local anaesthetic affinity of inactivated channels was develop
43 s available to facilitate a humane choice of anaesthetic agent for fish despite over 100 years of use
44                                       No one anaesthetic agent has emerged as best.
45 dergoing various levels of sedation with the anaesthetic agent propofol, replicating our results in t
46                     Propofol is primarily an anaesthetic agent, but its use in a sedative capacity ha
47 aesthesia with halothane and the alternative anaesthetic agent, sevoflurane.
48 anxiolytics, antidepressants, beta-blockers, anaesthetic agents and analgesics; length of sedation an
49 ity in a large series involving a variety of anaesthetic agents and techniques.
50                       Intravenous third-line anaesthetic agents are typically titrated in refractory
51          The approach of early escalation to anaesthetic agents for refractory generalised convulsive
52 respiratory dysfunction, differences between anaesthetic agents have emerged in systemic inflammation
53 nts confirm the above and also indicate that anaesthetic agents may offer some protection against the
54 tudy was to evaluate the impact of different anaesthetic agents on EGG in experimental pigs.
55        First, the cerebrovascular effects of anaesthetic agents used for neurological surgery are con
56  equipment, safer and more easily titratable anaesthetic agents, and possibly the practice of subspec
57 llowing treatments was critically evaluated: anaesthetic agents, anti-epileptic drugs, magnesium infu
58 ticity and cell death, and responsiveness to anaesthetic agents.
59 ensitivities to CO(2), lung inflation and/or anaesthetic agents.
60 the laboratory, exposed to three widely used anaesthetic agents.
61 bunits are required for direct activation by anaesthetics alone, and only one anaesthetic-sensitive s
62                Recent evidence suggests that anaesthetics also inhibit excitatory synaptic transmissi
63 n, focusing on three topics: choice of local anaesthetic and adjunct drugs, technical aspects and com
64 xide (N2O, laughing gas) has been used as an anaesthetic and analgesic for almost two centuries, but
65                       Ketamine is a valuable anaesthetic and analgesic that in recent years has gaine
66 ction in the radiology suite with obstetric, anaesthetic and neonatal teams in attendance.
67 e use of specialized assistants to undertake anaesthetic and peri-anaesthetic tasks.
68 odulate the inflammatory response, surgical, anaesthetic and pharmacological, may enhance recovery wi
69                                While several anaesthetics and analgesics have been reported to alter
70                                        Local anaesthetics and anti-epileptic drugs can suppress hyper
71                                 Most general anaesthetics and classical benzodiazepine drugs act thro
72 membrane stretch, arachidonic acid, volatile anaesthetics and heat.
73 the idea that TREK-1 is a target for general anaesthetics and neuroprotectants.
74 refractory status epilepticus), a variety of anaesthetics and nonpharmacological therapies can be adm
75 eptors that are contrastingly insensitive to anaesthetics and respond partially to several full GABA
76    Skin swabbing does not require the use of anaesthetics and triggers fewer changes in behaviour and
77                   Sodium channels bind local anaesthetics and various toxins.
78 erns about the neurotoxic potential of local anaesthetics and, in particular, of lignocaine.
79    The procedure is painful, requiring local anaesthetic, and is less effective against large lesions
80                                    Surgical, anaesthetic, and obstetric (SAO) health-care system stre
81 he surgical stress response, use of volatile anaesthetic, and opioids for analgesia.
82 ible phenomena observed in higher organisms, anaesthetics antagonize high-pressure signalling mediate
83 uch as antioxidant, anti-inflammatory, local anaesthetic, antinociceptive, cicatrizing, antiseptic, a
84 e subcortical nucleus, energetic response to anaesthetics appears to be affected by changes in both c
85 ensitive, and its ability to be activated by anaesthetics, arachidonic acid and internal acidosis rem
86 this may be that the mechanisms of action of anaesthetics are not fully understood.
87 ators, including benzodiazepines and general anaesthetics, are among the most successful drugs in cli
88  homomeric HCN1 channels is mediated through anaesthetic association with the membrane embedded chann
89                                         Both anaesthetics at each concentration also shifted the rela
90 ral information on the mechanisms of general anaesthetics at their physiological receptor sites is la
91 ceptors (GABAA Rs) by photolabelling with an anaesthetic barbiturate.
92       The method involves application of the anaesthetic benzocaine and intubation to maintain ventil
93                            We found that the anaesthetic benzocaine at 50 mg l(-1) was an effective a
94 es of GABA(A) receptors bound to intravenous anaesthetics, benzodiazepines and inhibitory modulators.
95  mutation (N395K) that lies within the local anaesthetic binding site of the channel.
96  signal transduction or as a component of an anaesthetic binding site per se is discussed.
97 a mutation (F216S), not located in the local anaesthetic binding site, had no effect on lidocaine inh
98 ping to fatigue before and after acute local anaesthetic block of the sympathetic nerves (stellate ga
99 e (F1579) in domain IV-S6, critical in local anaesthetic block, to alanine in QQQ (QQQ-F1579A) disabl
100                                        Local anaesthetics block pain through non-specific actions at
101                                        These anaesthetics block sodium channels and thereby the excit
102                        Most barbiturates are anaesthetics but a few unexpectedly are convulsants.
103                        Most barbiturates are anaesthetics but unexpectedly a few are convulsants whos
104 lays an important role in the action of most anaesthetics, but is thought to be especially relevant i
105  anaesthesia and rural setting for improving anaesthetic care in pregnant women.
106 r titles or abstracts mentioning surgical or anaesthetic care provision by associate clinicians or no
107 doscopy procedures performed under monitored anaesthetic care using propofol as a sedative agent can
108 d in patients receiving nitrous oxide as the anaesthetic carrier gas compared with those receiving ni
109 nts (approximately 1 aspiration/3000 general anaesthetic cases), gastric volume and pH have been used
110   RECENT FINDINGS: As well as the immediate 'anaesthetic' complications of pain, nausea and vomiting
111                                 For relevant anaesthetic composition (<5 % CO(2) ) and condition (hum
112  be safely delivered when titrating volatile anaesthetic concentrations using a processed electroence
113 ere told that they may or may not receive an anaesthetic cream on one arm.
114 e assessment sites was anaesthetised with an anaesthetic creme.
115 e depolarized potentials; on the other hand, anaesthetics decrease excitability by activating a TASK-
116 ensitive subunit is sufficient to confer the anaesthetic-dependent potentiation to the GABA current.
117 al benefits of intra-operative monitoring of anaesthetic depth and cerebral oxygenation as a pragmati
118            An association between increasing anaesthetic depth and decreased postoperative survival h
119                                   Control of anaesthetic depth has been reported using the median fre
120           Our trial defines a broad range of anaesthetic depth over which anaesthesia may be safely d
121                  Recently, the monitoring of anaesthetic depth using the bispectral index or auditory
122 ith action potentials blocked with the local anaesthetic derivative, QX-314.
123  seems unlikely that the actions of volatile anaesthetics described here are involved in the state of
124        Patient characteristics, surgical and anaesthetic details, and chart review at discharge were
125                High concentrations of either anaesthetic directly activated alpha6beta3gamma2L, but n
126 about risk and dealing with the aftermath of anaesthetic disasters are also reviewed specifically.
127    In contrast, no study showed an effect of anaesthetic doses (>100 mg kg(-1)) of ketamine on dopami
128 dies of the acute effects of ketamine at sub-anaesthetic doses for meta-analysis.
129 mined following application of different sub-anaesthetic doses of Ket.
130                                          Sub-anaesthetic doses of ketamine, a non-competitive N-methy
131 ll as what can be achieved without access to anaesthetic drugs at all.
132 n domains III and IV) was required for local anaesthetic drugs to modify Na+ channel gating currents,
133 ved with subanaesthetic doses of traditional anaesthetic drugs, as well as what can be achieved witho
134 hile reducing the administration and cost of anaesthetic drugs.
135 , time to perform the block, amount of local anaesthetics, duration of the block, need for supplement
136 transmitter release sites, thereby bypassing anaesthetic effects on channels and receptors in order t
137 e effects; transmitter action prevailed over anaesthetic effects on TASK channels, but not over effec
138  on channels and receptors in order to allow anaesthetic effects on the neurotransmitter release mach
139                     The halogenated volatile anaesthetic enflurane blocked both currents, but only th
140                       R-mTFD-MPPB, like most anaesthetics, enhanced receptor gating by rapidly bindin
141 he mechanisms through which volatile general anaesthetics exert their behavioural effects remain uncl
142                                    Simulated anaesthetic exposure reduced APD and ERP in both epicard
143  further gains in our understanding of local anaesthetic eye blocks and the management of patients un
144 travenous bolus) or saline adjunctive to the anaesthetic for the duration of their ECT course.
145                   This extends to the use of anaesthetics for both scientific study, humane killing a
146 flurane resulted in a ten-fold difference in anaesthetic gas emissions between hospitals.
147  its high cost because it is an almost ideal anaesthetic gas.
148 (>99+%) allows the use of the precious Xe as anaesthetics gas a viable general option in surgery.
149                                              Anaesthetic gases and energy consumption were the larges
150                                      General anaesthetics greatly impair thermoregulation, synchronou
151                                  The general anaesthetic halothane (1.5%) increased the oxygen-sensit
152 otonin (5-HT) and noradrenaline (NA)) and an anaesthetic (halothane) indeed compete for modulation of
153 (M314) upon allosteric regulation by general anaesthetics has been investigated.
154                                              Anaesthetics have been shown to exert both neurotoxic an
155       Although the molecular effects of many anaesthetics have been well characterized, a network-lev
156                                     Volatile anaesthetics have historically been considered to act in
157               Neurotransmitters and volatile anaesthetics have opposing effects on motoneuronal excit
158  conclusion, our data indicate that GABA and anaesthetics holistically activate the GABAA rho1 recept
159  to opioids, sedatives-hypnotics, or general anaesthetics in neonates (O-SH-GA).
160 tresses the importance of the choice of drug anaesthetics in order to avoid adverse effects on brain
161 little data exist to guide the withdrawal of anaesthetics in refractory status epilepticus.
162 inically relevant concentrations of volatile anaesthetics, including isoflurane.
163                                    All three anaesthetics increased the width of the tissue's vulnera
164 ce of seizures, whereas the prolonged use of anaesthetics increases the risk of treatment-associated
165 ively specific value of Ca(V)3.3 channels in anaesthetic induced hypnosis.
166 information on factors contributing to local anaesthetic induced neurotoxicity: adrenaline significan
167 re used to simulate the functional impact of anaesthetic-induced blockade of membrane currents on APD
168              We hypothesised that a volatile anaesthetic-induced decrease in myocardial contractility
169  the functional role of Ca(V)3.3 channels in anaesthetic-induced hypnosis and underlying neuronal osc
170 nder current clamp conditions, 5-HT reversed anaesthetic-induced membrane hyperpolarization and incre
171    Propofol has been an immensely successful anaesthetic induction agent but there is an increasing n
172 receive either methylprednisolone (250 mg at anaesthetic induction and 250 mg at initiation of cardio
173       Dexmedetomidine infusion, initiated at anaesthetic induction and continued for 24 h, did not de
174 ol, i.e. no injection) and between subjects (anaesthetic injection vs. saline injection).
175 ated the effectiveness of an intra-operative anaesthetic intervention in reducing post-operative cogn
176 ew describes the radiological, obstetric and anaesthetic interventions which are often carried out in
177        Measuring the direct drug costs of an anaesthetic is relatively easy, but assessing increased
178 administration of adequate concentrations of anaesthetics is not always feasible.
179  Etomidate, an intravenous imidazole general anaesthetic, is thought to produce anaesthesia by modula
180 e neurophysiological effects of the volatile anaesthetic isoflurane on axonal and synaptic function i
181  midazolam, propofol, ketamine, inhalational anaesthetics (isoflurane, desflurane), antiepileptic dru
182                       The antidepressant and anaesthetic ketamine (Ket) and four Ket metabolites were
183 ciousness to unconsciousness under different anaesthetics (ketamine and propofol).
184 e VTD receptor aligns closely with the local anaesthetic (LA) receptor, which resides at D1S6, D3S6 a
185 g studies have shown that lidocaine, a local anaesthetic (LA) that elicits depolarization-dependent (
186           It is also not known whether local anaesthetics (LAs) transferred to the fetal systemic cir
187 laboratory animals, exposure to most general anaesthetics leads to neurotoxicity manifested by neuron
188  is present in anaesthetized monkeys even at anaesthetic levels known to induce profound loss of cons
189 weaning may allow faster and more successful anaesthetic liberation after refractory status epileptic
190 tional connectivity emerge during successful anaesthetic liberation in status epilepticus; these find
191  intestinal mucosal application of the local anaesthetic lidocaine (lignocaine) or administration of
192 n extensive mutagenesis data, that the local anaesthetic lidocaine docks eccentrically below the sele
193 pecially relevant in the case of intravenous anaesthetics, like etomidate and propofol.
194 ew randomized studies are available to guide anaesthetic management but anaesthetists should aim to a
195              There is emerging evidence that anaesthetic management influences outcome.
196                        To review the current anaesthetic management of patients undergoing transthora
197 s review is to outline the priorities in the anaesthetic management of the child with facial abnormal
198 was to evaluate a potential influence of the anaesthetic method (inhaled anaesthetics versus total-in
199 s in some other solid tumours, the choice of anaesthetic method had no impact on survival in patients
200 test was used to assess the influence of the anaesthetic method.
201                                              Anaesthetic molecules act on synaptic transmission via t
202         VSTX1, small hydrophobic poisons and anaesthetic molecules reveal a common theme of voltage s
203 uvenile hair cells, unlike the commonly used anaesthetic MS-222, which reduces the size of basolatera
204                           Strikingly, either anaesthetic now activated the receptor, an effect confir
205 nRT neurones by enflurane and other volatile anaesthetics occurs within concentrations that are relev
206 nsating animals through superfusion of local anaesthetic on the round window.
207               The overall effect of volatile anaesthetics on the [Ca2+]i profile is likely to be dete
208         We studied the effects of inhalation anaesthetics on the membrane properties of hypoglossal m
209 ing and breathing were made within subjects (anaesthetic or saline injection vs. control, i.e. no inj
210 ion service to receive either awake-regional anaesthetic or sevoflurane-based general anaesthetic.
211 ents receiving either balanced with volatile anaesthetics or total intravenous anaesthesia were gener
212  pathway that permits the rapid diffusion of anaesthetics out of the Nav1.5 channel.
213                            He was completely anaesthetic over the entire left trigeminal distribution
214 od incorporating a miniature respiratory and anaesthetic perfusion set-up for live adult zebrafish, a
215 res of GABA(A) receptors in complex with the anaesthetics phenobarbital, etomidate and propofol revea
216 mechanism that governs internal QX and local anaesthetic pore block of voltage-gated Na+ channels and
217                This is a challenging area of anaesthetic practice but the use of a structured approac
218 ion, and training have had a major effect on anaesthetic practice, so that anaesthesia is increasingl
219 surgical patient is an integral part of good anaesthetic practice.
220                                              Anaesthetic preconditioning occurs when a volatile anaes
221 ween April 1, 2014, and Jan 31, 2015, 31 127 anaesthetic procedures in 30 874 children with a mean ag
222                           A total of 167,574 anaesthetic procedures were performed, including 158 cas
223  associate clinicians undertook surgical and anaesthetic procedures without supervision (100% for sur
224 bition of NCX-mediated Ca2+ efflux, volatile anaesthetics produce myocardial depression.
225 nits is inhibited by the intravenous general anaesthetic propofol (2,6-diisopropylphenol).
226 analgesia using paravertebral blocks and the anaesthetic propofol than with general anaesthesia with
227 tations of the conserved M1 proline, and the anaesthetic propofol, increase a rate constant for desen
228  sought to determine whether the intravenous anaesthetics propofol and etomidate inhibit the release
229    The time needed to train new surgical and anaesthetic providers was estimated with average length
230 forts to bridge the gap between surgical and anaesthetic providers.
231 d world, alternative indicators of obstetric anaesthetic quality are required.
232 ervice) investigates suspected perioperative anaesthetic reactions using serial tryptase, urinary met
233  or tactile stimuli and under four different anaesthetic regimens.
234                                           As anaesthetic-related maternal mortality reduces in the de
235                                              Anaesthetic research has the potential to further improv
236 Scottish Society of Anaesthetists, Edinburgh Anaesthetics Research and Education Fund.
237 nal excitability and are implicated in pain, anaesthetic responses, thermosensation, neuroprotection,
238 d influence pain, temperature perception and anaesthetic responses.
239 HCN1 channels in the absence and presence of anaesthetic reveals that (1) gating is best described by
240 epam and suggest an allosteric mechanism for anaesthetic reversal by flumazenil.
241                      Premature withdrawal of anaesthetics risks the recurrence of seizures, whereas t
242 ype and the mutated rho1 subunits, which are anaesthetic-sensitive and respond with full efficacy to
243 hen demonstrate that, in the pentamer, three anaesthetic-sensitive rho1 subunits are needed to impart
244 tivation by anaesthetics alone, and only one anaesthetic-sensitive subunit is sufficient to confer th
245                            By contrast, five anaesthetic-sensitive subunits are required for direct a
246 n with general anaesthesia with the volatile anaesthetic sevoflurane and opioid analgesia.
247                                           An anaesthetic should not induce negative behaviours and fi
248                      We recently located the anaesthetic sites on GABAA receptors (GABAA Rs) by photo
249 m its negligible affinity for the enhancing, anaesthetic sites.
250 nded cortical representation of adjacent non-anaesthetic skin does not influence the cortical process
251 st to adults, neuraxial blockade using local anaesthetic solutions is associated with stable cardiova
252 pidural space (which may mimic that of local anaesthetic solutions) appears to be highly variable, al
253 lpha-2-agonists have long been known to have anaesthetic-sparing, sedative and analgesic properties w
254  propofol can be recommended for use without anaesthetic staff.
255           Nitrous oxide is by far the oldest anaesthetic still in routine use and its continued use i
256 go the procedure and two had missing data on anaesthetic strategy), 236 (30%) of 797 patients who had
257                                     Volatile anaesthetics such as halothane, isoflurane and sevoflura
258                                        Local anaesthetics such as lidocaine (lignocaine) interact wit
259 though sodium channels are targeted by local anaesthetics such as lidocaine (lignocaine), some patien
260 s riluzole) and volatile and gaseous general anaesthetics (such as halothane and nitrous oxide).
261 hetic preconditioning occurs when a volatile anaesthetic, such as sevoflurane, is administered before
262  action in Drosophila, and suggest candidate anaesthetic target molecules.
263 ttractive model system for identification of anaesthetic targets.
264                   In contrast, return of pre-anaesthetic task performance was observed with a gradual
265                        Although surgical and anaesthetic task shifting has been described in many cou
266  global distribution and use of surgical and anaesthetic task shifting is needed to strengthen strate
267                                              Anaesthetic task shifting occured in 108 (65%) of 165 co
268 assistants to undertake anaesthetic and peri-anaesthetic tasks.
269  There are many different ways of organizing anaesthetic teams, in particular because the role of non
270    Neuropathic breast pain did not differ by anaesthetic technique and was reported by 87 (10%) of 85
271 advancements and innovations in surgical and anaesthetic technique have allowed us to offer surgical
272 tation with the patient, should decide which anaesthetic technique to use on an individual basis.
273 est managed by utilizing a total intravenous anaesthetic technique with propofol, the avoidance of ni
274 ent incisional breast pain was unaffected by anaesthetic technique.
275 reoperative risk assessment and surgical and anaesthetic techniques have resulted in a significant de
276 terized as PONV, at the very least, avoid an anaesthetic that may make PONV/PDNV worse and be aggress
277 gly different sensitivities to high doses of anaesthetics that suggest a hierarchy governing how the
278 and the number of cases reported for all non-anaesthetic therapies is low.
279 es or recurs 24 h or more after the onset of anaesthetic therapy, including those cases where status
280 nct to reducing the usage of potent volatile anaesthetics, thereby improving their safety.
281 ptic GABA(A)Rs to ambient GABA, alcohols and anaesthetics, these receptors may present a critical sit
282  of GABA via orthosteric sites, the force of anaesthetics through allosteric sites may not propagate
283 ury by injecting rhesus monkeys with a local anaesthetic to block the median and ulnar nerves at the
284 ced in the presence or absence of a volatile anaesthetic to selectively promote Ca2+ efflux via NCX.
285 ine at 50 mg l(-1) was an effective and safe anaesthetic to use on juvenile zebrafish.
286 mental effects of nitrous oxide derived from anaesthetic use are negligible and there is no convincin
287 0 [75.4 to 87.6], respectively) and volatile anaesthetic use was 0.26 minimum alveolar concentration
288                                   Most local anaesthetics used clinically are relatively hydrophobic
289                                              Anaesthetics used during cancer surgery may influence tu
290 and reflexology is a useful adjunct to local anaesthetic varicose vein surgery, with participants in
291 influence of the anaesthetic method (inhaled anaesthetics versus total-intravenous anaesthesia using
292 speed induction of anaesthesia with volatile anaesthetics, via a mechanism referred to as the "second
293                 We prespecified a successful anaesthetic wean as the discontinuation of intravenous a
294 ; these findings are absent in patients with anaesthetic wean failure.
295  accuracy of features of EEG activity during anaesthetic weaning in refractory status epilepticus as
296 fying features that emerge during successful anaesthetic weaning may allow faster and more successful
297                      Forty-seven consecutive anaesthetic weans (23 successes, 24 failures) were ident
298 nnectivity measures revealed that successful anaesthetic weans were characterized by the emergence of
299 l ketamine or clonidine as adjuncts to local anaesthetics will grow.
300 iable data on alternative short-acting local anaesthetics with respect to transient neurological symp

 
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